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首页> 外文期刊>Life sciences >Curcumin induces FasL-related apoptosis through p38 activation in human hepatocellular carcinoma Huh7 cells
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Curcumin induces FasL-related apoptosis through p38 activation in human hepatocellular carcinoma Huh7 cells

机译：姜黄素通过P38活化在人肝细胞癌HUH7细胞中诱导FasL相关的细胞凋亡

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摘要

Aim The aim of this study is to explore the underlying molecular mechanism of curcumin-induced apoptosis in human hepatocellular carcinoma (HCC) Huh7 cells. Main methods Fas and FasL mRNA expression was analyzed by reverse transcription PCR. Western blot was applied to detect the protein expression of Bcl-2 family members, MAPK family members, c-Jun, c-Fos, ATF-2, caspase-3, PARP, TNF receptor family members and the respective ligands. Apoptotic cells were assayed with annexin V/PI double staining and flow cytometry. Key findings Curcumin treatment resulted in a fast and significant increase of Fas and Fas ligand (FasL) along with activation of caspase-3 and cleavage of PARP in Huh7 cells. Inhibition of caspase-3 activity by the specific inhibitor Z-DEVD-FMK rescued Huh7 cells from curcumin-induced apoptosis. Neutralization of FasL significantly protected the cells from curcumin-induced caspase-3 activation and apoptosis in a dose-dependent manner. Moreover, p38 was rapidly activated in response to curcumin, and inactivation of p38 by pharmacologic inhibitor SB203580 dramatically suppressed curcumin-induced FasL expression and apoptosis. Significance Our results demonstrated that curcumin induces apoptosis through p38-denpendent up-regulation of FasL in Huh7 cells. ? 2012 Elsevier Inc. All rights reserved.
机译：目的本研究的目的是探讨姜黄素诱导的人肝癌（HCC）HUH7细胞中姜黄素诱导的细胞凋亡的潜在分子机制。通过逆转录PCR分析Fas和FasL mRNA表达的主要方法。应用Western印迹以检测Bcl-2家族，MAPK家族，C-JUM，C-FOS，ATF-2，Caspase-3，PARP，TNF受体家族成员和各自配体的蛋白质表达。用膜蛋白V / PI双染色和流式细胞术测定凋亡细胞。主要发现姜黄素处理导致Fas和Fas配体（FasL）的快速显着增加，以及Caspase-3的激活并在Huh7细胞中切割PALP。通过特异性抑制剂Z-Devd-FMK抑制Caspase-3活性的抑制来自姜黄素诱导的细胞凋亡的HUH7细胞。 FasL的中和显着保护从姜黄素诱导的Caspase-3激活和细胞凋亡以剂量依赖性方式保护细胞。此外，响应于姜黄素迅速激活P38，并通过药理学抑制剂SB203580的P38失活显着抑制了姜黄素诱导的FasL表达和凋亡。重要意义我们的结果表明，姜黄素通过P38-Denpendent对HUH7细胞的FasL诱导细胞凋亡。还是2012年Elsevier Inc.保留所有权利。

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  • 来源
    《Life sciences》 |2013年第7期|共7页
  • 作者

    WangW.-Z.; LiL.; LiuM.-Y.; JinX.-B.; MaoJ.-W.; PuQ.-H.; MengM.-J.; ChenX.-G.; ZhuJ.-Y.;

  • 作者单位

    Guangdong Province Key Laboratory of Pharmaceutical Bioactive Substances Guangdong Pharmaceutical;

    Department of Hematology Guangzhou General Hospital of Guangzhou Military Area Command of Chinese;

    Guangdong Province Key Laboratory of Pharmaceutical Bioactive Substances Guangdong Pharmaceutical;

    Guangdong Province Key Laboratory of Pharmaceutical Bioactive Substances Guangdong Pharmaceutical;

    Guangdong Province Key Laboratory of Pharmaceutical Bioactive Substances Guangdong Pharmaceutical;

    Guangdong Province Key Laboratory of Pharmaceutical Bioactive Substances Guangdong Pharmaceutical;

    Guangzhou Higher Education Mega Center Health Industrial Science Technology Park Investment;

    School of Pubic Heath and Tropical Medicine Southern Medical University Guangzhou China;

    Guangdong Province Key Laboratory of Pharmaceutical Bioactive Substances Guangdong Pharmaceutical;

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  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类 医药、卫生;
  • 关键词

    Apoptosis; Curcumin; FasL; Huh7 cells; p38;

    机译：细胞凋亡;姜黄素;FasL;HUH7细胞;P38;

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